Chronic diarrhea, an ubiquitous problem in captive colonies of nonhuman primates, is associated with a complex of physiologic changes resulting in a high incidence of morbidity and mortality. Although a variety of bacterial, viral, parasitic, and fungal agents has been implicated in the etiology of diarrheal disease, the majority of chronic diarrheas in these animals are idiopathic. The large intestine is the site most often altered in macaques affected by idiopathic chronic diarrheal disease (ICDD) with the primary lesion being a dense inflammatory infiltrate of the lamina propria comprising lymphocytes, plasma cells, and histiocytes with lesser numbers of neutrophils and eosinophils. Associated changes include goblet cell depletion, crypt dysplasia, attenuation/disruption of the surface epithelium, and "crypt abscesses" containing neutrophils and necrotic debris. Ulcerative colitis (UC) is an idiopathic inflammatory bowel disease affecting humans; the lesions share some of the features of ICDD in macaques. The similarities between uc in humans and icdd in rhesus macaques make the latter a potential animal model of the human disease. Detailed characterization of the inflammatory infiltrate present in UC, but not ICDD, has been performed. Identification of the phenotypes and relative numbers of mononuclear leukocytes in the lamina propria of rhesus macaques with ICDD would help to substantiate the validity of ICDD as an animal model of human UC. Immunohistochemical techniques using monoclonal antibodies to surface markers on macrophages, T-lymphocytes, and the helper (cd4) and suppressor (cd8) subsets of T-cells, as well as antibodies to various adhesion molecules have been used to study inflammation in ICDD of macaques. Results indicate that the normal cd4:cd8 ratio in the colonic lamina propria of macaques is similar to that in humans and that this ratio increases in macaques with ICDD. Furthermore, antibodies to human adhesion molecules cross-react with those of macaques.